histopathology of caries :) Flashcards
clincial types of cariees
acute
chronic
arrested
what is acute caries
caries which is extensive
affects flat surfaces of the teeth (ie front of incisors)
what is chronic caries
occlusal caries
what is arrested caries
caries has stopped due to a change in environment
part of the mouth has become self cleaning
what does ground sectons allow us to look at
hard parts of the tooth
cannot preserve soft tissue
demineralised sections
organic matrix left
cannot see enamel
normal enamel
prisms prism borders cross striations straie of retizus surface zone
straie of retizus
more pronounced incremental lines
what causes incremental lines
ameloblasts stop and rest and then move in a different direction
where does demineralisation generally start and why
prism borders
cross straitions
straie of retizus
- have more organic matrix allowing acid to enter
sites for caries
smooth surface
fissur
root/cementum
recurrent (caries under a restoration)
types of arrested caries
type 1 and type 2
what is type 1 arrested caries
advanced dentine lesion becomes self cleaning
what is type 2 arrested caries
white spot enamel lesion may remineralise
where does root/cementum caries usually start
ACJ - where enamel meets cementum
where is root caries seen
proximal and buccal root surfaces
can have multiple lesions on same tooth
caries on cemntum/dentine
poorly resistance
PDL fibres allow rapid spread to dentine
caries will progress apically due to tubules in dentine
classifications of pulp pathology
inflammatory
degenerative
what is inflammatory pulp pathology
pulpitis ie pulp inflammtio
types of degenerative pulp pathology
fibrosis
calcifications
internal resorption
forms of pulpitis
acute
chronic
then within these are open and closed
what is open pulpitis
pulp is open to orla envionrment
what is closed pulpitis
enamel is still in tact, pulp not exposed
causes of pulpitis
infection -dental caries - cracked teeth - transient bacteriamia trauma physcial, mechanical, chemical
what happens is the pulp is not treated
die by necrosis
what happens after the pulp begins to die by necrosis
inflammatory process starts at the apex of the root
types of periapicla pathology
periapical periodontis (inflammatory) reactive - hypercementosis - ankylosis - osteoscelrosis
causes of periapical pathology
infection (vie root canal, periodontium or bacteriamia)
trauma (chemical, physical, mechanical)
what can pulpitis least to
formation of a cyst
what is the earliest evidence of a carious lesion on a smooth surface
white/brown spot
where is a lesion most likey to form on a premolar tooth
below the contact point between teeth where palaque can stagnante and collect
why may lesions be brown instead of white
enamel increases in porosity and then pigment of food wll be absorbed
how can an early carious lesion be fixefd
enamel is still in tact and can be remineralsied
- removal of plawue
- apply fluride
- improve OH
what can happen at the ADJ
laterla spread of caires
acid can spread more easily
what 4 zones are there within the enamel lesion
translucent zone
dark zone
body of lesion
surface zone
what is the largest zone in the enamel lesion
body of lesion
what do the zones relate to
enamel porisity
what zone has the greatest porosity
body
what porosity results in cavitation
20-25%
body can no longer support the surface lesion
how does porosity increase
movement of calcium out of the tooth
hydroxyapitite mineral is being dissolved out of the enamel
translucent zone
advancing edge of lesion
small number of large pores
demineralisation at the edgeof prisms
in 50%of lesions
dark zone
85-85% lesions varible in thickness narrower =more rapid advance more pores but smaller than TZ represents re-precipitation of minerals dissolved out in TZ
body of lesion
demineralisatio of prism cores
pore volume 20% centre 5% edge
some amount of reprecipitation
surface zone
unaffected layer
incontact with surface biofilm
resisits demineralisation until dentine involved
dynamic process of de/remineralsiation
acid influxes results into demineralisation and movement of CA out
fluride favours reminerlisation
(calcium moves in)
earliest clinical evidence in enamel fissure caries
white opacit around fissure paerure
may be sticky brown spot
shape of fissure caries and where do they arise and spread
conical lesion with base towards ADJ
lesion arise in fissure walls
spread at ADJ
how does fissure caries progress into dentine (types)
priamry enamel caries - lateral spread at ADJ secondary enamel caries - careis extends backwards early dentine caries - acid diffuses to dentine
what respond toether as a compelx
dentine and pulp
how does the dentine and pulp respond to caries
dentine tubules run from ADJ to the pulp
the tubules are closed off in responce
what are defence reactons of plaque acid
tertiary dentine
scelrotic entine
dead tracts
tertiary dentine
closes off the tubules at the pulp end and make more dentine
sclerotic dentien
fill in the tubules
mineralisation of odontoblast processes
dead tracts
empty tubules sealed at th end and filled with air
odontoblast death
what the the shapeof caries affected by
site
ie fissure vs smooth surface
dental caries before cavitation
acid diffuses through intact porous enamel
pulp dentine unit repspods
what are the two main zones before cavitation
scelortic zone (around the outside) body of lesion (deminerlised)
how does cavitation occur
surface enamel no longer able to structurally support itself
(carious enamel collapses_
what happens after bactera has entered the dentine
1st wave - aidogenic bactera enter, demineralise enamel and dentine
2nd wave
colonisation of different bacteria
mixed popilation produce proteolytic enzymes that destroy demineralisaed collagen matrix
what do bacteria do in the dentine tubules
mulitply in the tubules which widen and collapse
‘liquefaction foci’
what does collapsing of dentine tubles lead to
expansion and formation of dentine clefts
thes can flake off (point of weakness)
what is the body of the lesion subdivied into
demineralisation
bacterial penetration
destruction
what is in the demineralisation part of the body of the cavitation
dentine has lost mineral but still has tubular structure
no bacteria and dentine is stained
what is in the bacteria penetration of the body
bacteria multiply in tubles
infected soft dentine
stil maintains some tubular matrix
describe the destruction in the body
base of cavity
discoloured
liquefaction foci and transverse clefts
where is the head of the scleotic zone
near the pulp
what happens to the pulp upon caries advancing
pulp tries to shrink away from caries
odontoblasts wrking hrder to make dentine more quickly
tertiary dentine increasing in irregularity
pulp inflammation increases
bacteria invade tertiary dentine and reach pulp
